Cardiopulmonary monitoring of clinically unstable patients is essential for early detection of potentially life threatening changes in the functionality of the heart or respiration. Cardiopulmonary monitoring is presently done on hospitalized patients in critical care, such as intensive care units (ICU), coronary care units (CCU) and peri-operatively as well as in other specialized sections of the hospital. Certain types of cardiopulmonary monitoring are also performed on patients outside the hospital, such as patients who suffer from asthma, high blood pressure, or cardiac arrhythmias. Cardiopulmonary monitoring is also used during exercise performance tests of patients and athletes. Clearly, monitoring and early detection of impending catastrophes are highly desirable in clinical medicine.
Continuous monitoring of cardiopulmonary wellbeing is presently focused on physiological parameters that characterize, individually, the activity of the heart and respiration. These parameters include monitoring of the electrocardiogram, blood pressure in the arterial, venous and pulmonary circulations and cardiac output for assessing the cardiovascular system. The airway pressure, respiratory rate, tidal volume, flow rate, pulse oximetry, exhaled CO2, and esophageal pressures are the respiratory parameters that are commonly monitored. More recently continuous overnight monitoring of breath sounds was introduced to detect and quantify wheezing activity in asthmatics. Additional methods were introduced to monitor patients inflicted with congestive heart failure (CHF) to identify early decompensation. These methods are based on continuous monitoring of the electrical impedance of the thorax, but have not generated reliable levels of sensitivity and specificity. Monitoring of respiratory crackles has also been used as an early sign of lung congestion.
The activities of the heart and the lungs are well known to be closely interrelated. The heart rate, blood pressure and blood flow into and out of the heart are influenced by the breathing cycle. The pressure inside the chest becomes more negative during inspiration to enable inflow of air into the lung alveoli. This sub-atmospheric pressure also affects the heart, blood vessels and blood flow. In particular, the increased intrathoracic negative pressure expands the right atrium and ventricle, dilates and elongates the blood vessels, amplifies the ventricular filling and changes the position of the inter ventricular septum. In addition, the changes in lung volume modify the afferent neuronal activity in the vagus nerve, leading to modulation of the heart rate during respiration. During quiet breathing the intrapleural pressure decreases from about −3 mm Hg to about −6 mm Hg. This causes dilation of the intrathoracic segment of the vena cava, increased venous return to the right atrium and ventricle. The increased diastolic filling of the right ventricle amplifies its stroke volume into the pulmonary circulation by the well-known Starling mechanism. At the same time, the inspiratory displacement of the abdominal content by the contracting diaphragm increases the intra abdominal pressure, which further pushes blood into the thoracic cavity. The intrathoracic pressure changes during breathing also influence the output of the left ventricle, but to a lesser degree. During deep breathing, or in pulmonary diseases that affect the mechanical properties of the airways and the lung parenchyma these, respiratory swings of flow, resistance and volume are greatly exaggerated (Mountcastle V. O. Medical Physiology, 12th ed. Mosby Company, St. Louis 1968).
Positive pressure ventilation squeezes the pulmonary capillaries and increases the resistance to blood flow through the lungs. These pressures may diminish the output of the right ventricle due to increased afterload, while at the same time reducing the output of the left ventricle due to fall in its diastolic filling and preload. These phenomena are known to result in wide fluctuations of the cardiac output and blood pressure. Similar fluctuations are also seen during resisted breathing, cough and isometric muscle straining.
Monitoring of heart sounds is well known to medicine and physiology for many years, even before the invention of the stethoscope by Laennec in 1819. The first and second heart sounds are associated with closing of the atrioventricular and ventricular outlet valves, respectively. They are loud and distinct sounds with somewhat different amplitude and template in different areas of precordial auscultation. The first and second heart sounds are modified, and sometimes are even completely missing during diseases of the heart or the lungs. Additionally, the 3rd and 4th heart sounds are well known to be associated with defects of the left ventricular filling during diastole. Rumbling sounds heard in between the first and second sounds (systole) or the second and first sounds (diastole) are appropriately called systolic and diastolic murmurs, respectively and are associated with abnormal blood flow through the narrowed or malfunctioning heart valves. Information on heart sounds, phonocardiography and the art of interpretation of heart sounds is readily available in many text books and articles, such as in “Rapid interpretation of heart sounds and murmurs” by Emanuel Stein, Abner J. Delman (Editors), Williams & Wilkins, 1997, 4th edition, the contents of which are incorporated herein by reference.
The respiratory changes of cardiac activity are well known. In particular, the phenomenon of “Pulsus Paradoxus” is a recognized sign of severe asthma and airway narrowing. It is defined as a decline of greater than 12 mm Hg (in some texts 20 mm Hg) in the systolic blood pressure during inspiration. Detection of Pulsus Paradoxus in a dyspneic patient is an ominous sign that calls for aggressive and immediate intervention. On the other hand, cardiac arrhythmia, the acceleration and deceleration of the heart rate during the respiratory cycle is often a benign and normal phenomenon, particularly in young children. The only available information on the effect of respiration on the heart sounds per-se is on the width of splitting of the second heart sound and on certain cardiac murmurs. Otherwise, no information is available on the changes in the heart sounds induced by respiration and on the extent of these changes during various cardiopulmonary conditions.
The failing heart condition is a cause for severe morbidity and mortality rates. This condition can be helped by a broad range of assist methods. These include pharmaceutical agents (e.g., digitalis and other positive inotropic agents), mechanical support (e.g., intra aortic counter pulsation, and intravascular coronary artery stent), and various types of electrical stimulation (e.g., ventricular resynchronization therapy, Guidant's Contak CD, Medtronic's multi electrode epicardial pacing, Impulse Dynamics' timed refractory period current). All heartbeat synchronized methods must be monitored as regards their performance. This feedback can determine if, and to what extent the assistance is effective. Such monitoring is either performed in intervals (e.g., by periodic determination of the left ventricular ejection function), or continuous (e.g., by monitoring the left ventricular pressure—Remon Medical Technologies LTD of 7 Halamish Street, Caesaria Industrial Park, 38900, Israel). To be effective, the mechanical and electrical assist methods should be synchronized with the cardiac cycle so that they can be activated at specific phases of the cardiac cycle. For example, in U.S. Pat. No. 6,285,906 the contents of which are incorporated herein by reference, impulse dynamics provides current stimuli at certain precise phases of the heart cycle. To do so, most methods use the EKG (electrocardiographic) signal to find the appropriate timing within the cardiac cycle for activation of the assistance. However, the EKG may not provide sufficiently detailed or accurate information about the timing cardiac cycle, or may be contaminated by electromagnetic noise.